Classical Swine Fever

Description

Classical swine fever is a highly contagious, haemorrhagic disease of swine which is caused by a Togavirus. Presentation may be actue, sub-acute, chronic or persistent, and the disease is indistinguishable in the field from African Swine Fever. Acutely, classical swine fever is characterised by severe depression, high fever and superficial and internal haemorrhages, with many cases resulting in death. Depression, anorexia and pyrexia are seen in chronic classical swine fever. Transplacental infection is also possible and results in persistently infected piglets.

Aetiology

The causative agent of classical swine fever is a small, enveloped virus of around 40nm diameter. The genome is comprised of single stranded RNA, which is positive sense and contains about 12,300 bases. The sequence of the genome is known, and codes four structural and seven non-structural proteins. The classical swine fever virus is relatively stable in excretions and in fresh meat products including ham, salami and other similar sausages. It is, however, easily inactivated by detergents, common disinfectants and heat.

Classical swine fever virus is a Togavirus within the Pestivirus genus of the Flaviviridae. As such, it is closely related to the bovine viral diarrhoea (BVD) virus of cattle, and the border disease virus of sheep.

Signalment

Domestic pigs and other swine of any age may become infected with classical swine fever.

Pathogenesis

Infection is by aerosol contact or direct spread. Entrance is through skin abrasions or mucous membranes. The incubation is usually 3-4 days (but may vary to 5-10 days). Virus infects epithelial cells of tonsillar crypts and subsequently spreads to regional lymph nodes via lymphatics. It enters the blood stream, replicates in the spleen, bone marrow and lymph nodes. Multiple haemorrhages are caused by degeneration of endothelial cells of blood vessles and thrombocytopaenia resulting in poor blood coagulation. In acute CSF, pigs die from the acute angiopathy, shock and febrile response. Pigs that survive develop a chronic form of the disease with enteric and joint lesions that are the result of tissue infarction. Piglets infected in utero are born persistently infected. They grow poorly and excrete virus over long periods.

A major area of recent study has been the nature of the interaction between virus and host and attempts to Research in Veterinary Science 75 (2003) 169–178 www.elsevier.com/locate/rvsc

• Corresponding author. Tel.: +44-1483-231012; fax: +44-1483-

232621. E-mail address: david.paton@bbsrc.ac.uk (D.J. Paton). 0034-5288/$ - see front matter � 2003 Elsevier Science Ltd. All rights reserved. doi:10.1016/S0034-5288(03)00076-6 understand how the virus is able to avoid the innate immune system, delay the onset of acquired immunity and produce its pathogenic effects. Like other pestiviruses, CSFV grows readily in vitro and is able to cause a persistent, non-cytopathic infection of cell cultures. This indicates that the virus can avoid the antiviral effects of type I interferon and prevent programmed cell death (apoptosis). Indeed, porcine cells infected with CSFV are strongly protected against stimuli that normally trigger apoptosis, such as treatment with double-stranded RNA, and resist the antiviral effects of type I interferon (Ruggli et al., 2002). The first protein encoded by the genome, Npro, is an autoprotease that cleaves itself from the nascent viral polyprotein and whose function has been enigmatic. Recently, it has been shown that CSFV, lacking Npro induces rather than inhibits an interferon response in infected monocytes (Ruggli et al., 2002). CSFV is also immunosuppressive and neutralising antibodies may not appear until three weeks after infection. Since the virus is so innocuous in vitro, it has long been suspected that the serious lesions found in vivo must have an immunopathological origin. During infection, there are profound changes in the bone marrow and in the circulating white cell population and these may precede widespread infection of these cell types (Knoetig et al., 1999; Summerfield et al., 1998, 2001a). This suggests an indirect cytopathic effect induced in mainly uninfected cells, damaged by a soluble viral factor or by some other disturbance of cellular homeostasis. There is evidence for both of these mechanisms. Firstly, there is a soluble viral protein Erns that at high concentrations is able to induce apoptosis in lymphocytes in vitro (Bruschke et al., 1997). However, supernatant fluids collected from cell cultures infected with CSFV do not induce apoptosis (Summerfield et al., 2001b). Secondly, virus replication in monocytes and macrophages induces the release of cytokines including prostaglandin-E2 and interleukin-1, which have a probable role in fever and haemorrhages (Knoetig et al., 1999). Although the majority of pestiviruses are noncytopathic in vitro, BVD viruses from cases of mucosal disease and a small minority of CSF viruses can be cytopathic in vitro, expression of NS3 being the hallmark of such cytopathic viruses (Kummerer et al., 2000).

Treatment

Control

• NOTIFIABLE disease
• Vaccination (live attenuated) in endemic countries:
  • Parts of EU are using vaccinated bait to control spread in wild boar population
  • Vaccination does not curtail spread: marker vaccine needed to distinguish virus exposure from vaccine-induced antibody